Immunosuppressant agent FK506 stimulates growth hormone (GH) secretion and gene expression of hypothalamic GH-releasing hormone in the rat.

Murao, Koji; Sato, Makoto; Niimi, Michio; Wada, Yoshinaru; Matsubara, Seishiro; Takahara, Jiro

doi:10.1210/endo.137.3.8603582

Cited by 6 publications

(4 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our results and previous reports indicate that both the protein kinase A and PI3-K/Akt pathways regulate the expression of hSR-BI/CLA-1. In support of this possibility, the sequence of the hSR-BI/CLA-1 promoter contains binding sites for transcription factors shown to participate in cross-talk between signal transcription and gene regulation (31). Further studies will be needed to determine the detailed regulatory mechanisms on hSR-BI/CLA-1 gene.…”

Section: Fig 5 Decreased Level Of Hepatic Sr-bi Mrna In Igf-i-treatmentioning

confidence: 98%

See 1 more Smart Citation

Insulin-Like Growth Factor-I Regulation of Hepatic Scavenger Receptor Class BI

Cao¹,

Murao²,

Imachi³

et al. 2004

Endocrinology

View full text Add to dashboard Cite

High-density lipoprotein mediates a normal physiological process called reverse cholesterol transport. This process enables the transfer of cholesterol from peripheral tissues to the liver for further metabolism and eventual secretion in the form of bile. The scavenger receptor of the B class (SR-BI), human homolog of SR-BI, and CD36 and LIMPII analogous-1 (CLA-1) are different names for the same receptor that facilitates hepatocellular uptake of cholesterol from high-density lipoprotein. The pivotal role of this receptor in enterohepatic circulation of cholesterol and bile salts underlies our interest to study the regulation of hepatic SR-BI gene in response to the actions of IGF-I. The results of our studies showed that endogenous expression of SR-BI/CLA-1 was suppressed by exposure to GH or IGF-I in cultured HepG2 cells. This observation extended to a whole animal model of rats continuously infused with IGF-I. IGF-I decreased transcriptional activity of the SR-BI promoter. However, the inhibitory effect of IGF-I on SR-BI/CLA-1 promoter activity was abrogated by wortmannin, a specific inhibitor of phosphoinositide 3-kinase (PI3-K). Exposure of HepG2 cells to IGF-I elicited a rapid phosphorylation of Akt. We also demonstrated that the constitutively active form of both p110, a subunit of PI3-K, and Akt inhibited activity of the human SR-BI/CLA-1 promoter. Furthermore, the dominant-negative mutant of Akt abolished the ability of IGF-I to suppress activity of the SR-BI/CLA-1 promoter. In conclusion, PI3-K/Akt pathways participate in IGF-I-suppression of SR-BI/CLA-1 expression, which suggests that the activation of Akt plays an important role in cholesterol metabolism in liver.

show abstract

Section: Fig 5 Decreased Level Of Hepatic Sr-bi Mrna In Igf-i-treatmentioning

confidence: 98%

“…Electrophoresis and hybridization were performed as described (30). Blots were also probed with human GAPDH to ensure equal loading of the RNA samples (31). After autoradiography at room temperature for 24 h, hybridization signals were detected using a Bioimaging Analyzer (BAS 1000; Fuji Photo Film, Tokyo, Japan).…”

Section: Northern Blot Analysismentioning

confidence: 99%

Insulin-Like Growth Factor-I Regulation of Hepatic Scavenger Receptor Class BI

Cao¹,

Murao²,

Imachi³

et al. 2004

Endocrinology

View full text Add to dashboard Cite

show abstract

“…The results were expressed as ng per ml NIDDK rat CH RP-2. The pulsatile pattern of CH secretion during the 6-h period was analyzed with the Detect program [20] which calculates the number of hormone pulses, their peak height and their duration. Pituitary GRH receptor mRNA levels…”

Section: Dex Treatment and Measurement Of Spontaneous Gh Secretionmentioning

confidence: 99%

Effects of Short- and Long-Term Dexamethasone Treatment on Growth and Growth Hormone (GH)-Releasing Hormone (GRH)-GH-Insulin-Like Growth Factor-l Axis in Conscious Rats.

et al. 1997

View full text Add to dashboard Cite

Abstract. Although the inhibitory effects of a chronic excess of glucocorticoids (GC) on body growth and GH secretion are well established, the mechanisms involved remain unclear. In this study, we examined the chronic effects of a high dose of dexamethasone (DEX) on spontaneous GH secretion and insulin-like growth factor (IGF)-I in conscious rats. The animals were given daily ip injections of DEX (200 µg/day) for either one or four weeks. Body growth assessed by tibia length and serum IGF-I levels was significantly inhibited 1 week after treatment. By contrast, spontaneous GH secretion was not altered 1 week after the treatment. Neither hypothalamic GRH and somtatostain mRNA levels nor GH responses to GRH from single somatotropes were affected 1 week after the treatment. Four weeks after DEX treatment, body growth of the rats was noticeably suppressed.Interestingly, spontaneous GH secretion, hypothalamic GRH mRNA levels and GH responses to GRH were all inhibited 4 weeks after treatment. Pituitary GRH receptor mRNA levels were not altered 1 week after treatment, but increased after 4 weeks. These results indicate that a high dose of DEX initially impairs IGF-I production and subsequently inhibits spontaneous GH secretion in rats. Inhibition of spontaneous GH secretion resulting from chronic GC excess is due, at least in part, to the impairment of hypothalamic GRH synthesis and pituitary GH responsiveness. An increase in the pituitary GRH receptor may be caused by decreased GRH secretion.

show abstract

“…Electrophoresis and hybridization were performed as described previously (13). Blots were also probed with rat ␤-actin to assess equal loading of samples (14). After autoradiography at room temperature for 24 h, hybridization signals were detected using a Bioimaging Analyzer (BAS 1000; Fuji Photo Film, Tokyo, Japan).…”

Section: Northern Blot Analysismentioning

confidence: 99%

Thyrotropin-Releasing Hormone-Stimulated Thyrotropin Expression Involves Islet-Brain-1/c-Jun N-Terminal Kinase Interacting Protein-1

Abe¹,

Murao²,

Imachi³

et al. 2004

Endocrinology

View full text Add to dashboard Cite

Islet-brain-1 (IB1)/c-Jun N-terminal kinase interacting protein 1 (JIP-1) is a scaffold protein that is expressed at high levels in neurons and the endocrine pancreas. IB1/JIP-1 interacts with the c-Jun N-terminal kinase and mediates the specific physiological stimuli (such as cytokines). However, the potential role of the protein in the pituitary has not been evaluated. Herein, we examined expression of the gene encoding IB1/JIP-1 and its translated product in the anterior pituitary gland and a pituitary cell line, GH3. We then examined the potential role of IB1/JIP-1 in controlling TSH-beta gene expression. Exposure of GH3 cells to TRH stimulated the expression of IB1/JIP-1 protein levels, mRNA, and transcription of the promoter. The increase of IB1/JIP-1 content by transient transfection study of a vector encoding IB1/JIP-1 or by the stimulation of TRH stimulates TSH-beta promoter activity. This effect is not found in the presence of a mutated nonfunctional (IB1S59N) IB1/JIP-1 protein. Together, these facts point to a central role of the IB1/JIP-1 protein in the control of TRH-mediated TSH-beta stimulation.

show abstract

Immunosuppressant agent FK506 stimulates growth hormone (GH) secretion and gene expression of hypothalamic GH-releasing hormone in the rat.

Cited by 6 publications

References 25 publications

Insulin-Like Growth Factor-I Regulation of Hepatic Scavenger Receptor Class BI

Insulin-Like Growth Factor-I Regulation of Hepatic Scavenger Receptor Class BI

Effects of Short- and Long-Term Dexamethasone Treatment on Growth and Growth Hormone (GH)-Releasing Hormone (GRH)-GH-Insulin-Like Growth Factor-l Axis in Conscious Rats.

Thyrotropin-Releasing Hormone-Stimulated Thyrotropin Expression Involves Islet-Brain-1/c-Jun N-Terminal Kinase Interacting Protein-1

Contact Info

Product

Resources

About